Analysis of pulmonary effluent from 105 preterm and term human neonates for constituent cytologic, protein, and phospholipid components are being performed throughout the period of neonatal pulmonary disease. We have defined the tracheo-pulmonary cytologic characteristics of acute respiratory distress syndrome and resolution of this disorder when compared to age matched controls requiring ventilatory support for non-pulmonary disorders. Development of bronchopulmonary dysplasia, a chronic lung disorder, has further been defined and classified according to predominance of cellular composition in bronchial secretions. Pulmonary surface active phospholipid profiles were performed sequentially throughout the course of recovery from respiratory distress syndrome. We have demonstrated a rise in the proportions of dipalmitoyl phosphatidylcholine and phosphatidylinositol in preterm infants. In preterm (less than 32 weeks) neonates, phosphatidylinositol content remains elevated until the 10-14th postnatal day when phosphatidylglycerol appears. We have not, as yet, defined differences in the appearance of these phospholipids in infants developing bronchopulmonary dysplasia and those not developing this complication. During exposure to supplemental oxygen (FiO2 greater than .8), for up to 77 hrs., alpha and beta fatty acid composition of the major phospholipids shifts to a majority of saturated forms on PC, PI, but not PG. Further efforts to define characteristic proteins in the pulmonary effluent and alterations in effluent proteins during oxygen exposure continue. Evaluation of effluent polyphosphoinosites are continuing and will be the focus of the 02 year.